ST Elevation Myocardial ST Elevation Myocardial Infarction (STEMI)Infarction (STEMI)

William J. Mosley II, MDWilliam J. Mosley II, MDCardiovascular Disease FellowCardiovascular Disease Fellow

(Updated from John Rapp with 2007 (Updated from John Rapp with 2007 guidelines)guidelines)

ACS-STEMIACS-STEMI

ACUTE CORONARY SYNDROMES

No ST elevation ST elevation

Unstableangina

NSTEMI STEMIStableangina

OutlineOutline

•Class/EvidenceClass/Evidence

•General TherapyGeneral Therapy

•Beta-blockersBeta-blockers

•ReperfusionReperfusion

•Facilitated PCIFacilitated PCI

•ComplicationsComplications

Class I Benefit >>> Risk

Procedure/ Treatment SHOULD be performed/ administered

Class IIa Benefit >> RiskAdditional studies with focused objectives needed

IT IS REASONABLE to perform procedure/administer treatment

Class IIb Benefit ≥ RiskAdditional studies with broad objectives needed; Additional registry data would be helpful

Procedure/Treatment MAY BE CONSIDERED

Class III Risk ≥ BenefitNo additional studies needed

Procedure/Treatment should NOT be performed/administered SINCE IT IS NOT HELPFUL AND MAY BE HARMFUL

Applying Classification of Recommendations and Level of Evidence

Level A: Recommendation based on evidence from multiple randomized trials or meta-analyses Multiple (3-5) population risk strata evaluated; General consistency of direction and magnitude of effect

Level B: Recommendation based on evidence from a single randomized trial or non-randomized studies Limited (2-3) population risk strata evaluated

Level C: Recommendation based on expert opinion, case studies, or standard-of-care Very limited (1-2) population risk strata evaluated

Hospitalizations in the U.S. Due to Acute Coronary Syndromes (ACS)

Acute Coronary Syndromes*

1.57 Million Hospital Admissions - ACS

UA/NSTEMI† STEMI

1.24 million Admissions per year

.33 million Admissions per year

Heart Disease and Stroke Statistics – 2007 Update. Circulation 2007; 115:69-171. *Primary and secondary diagnoses. †About 0.57 million

NSTEMI and 0.67 million UA.

General TherapyGeneral Therapy

General TherapyGeneral Therapy

• MONAMONA– Morphine (Morphine (q 5-15 min CLASS I)– Oxygen (Oxygen (pulse ox>90% CLASS I)– Nitroglycerin (Nitroglycerin (0.4 mg SL NTG x 3 for

ischemic pain CLASS I)– AspirinAspirin

AspirinAspirin• Aspirin should be chewed by patients who have not

taken aspirin before presentation with STEMI. The initial dose should be 162 mg (Level of Evidence: A) to 325 mg (Level of Evidence: C). Class I

• In a dose of 162 mg or more, aspirin produces a rapid clinical antithrombotic effect caused by immediate and near-total inhibition of thromboxane A2 production. (ISIS-2-->ASA led to 23% reduction in mortality):

1. Antithrombotic Trialists’ Collaboration. Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ. 2002; 324: 71–86.

2. ISIS-2 (Second International Study of Infarct Survival) Collaborative Group. Randomised trial of intravenous streptokinase, oral aspirin, both, or neither among 17187 cases of suspected acute myocardial infarction. Lancet 1988;ii:349-60.

Beta-BlockersBeta-Blockers

INCLUSION:INCLUSION: >45,000 patients with suspected acute >45,000 patients with suspected acute MI (ST change or LBBB) within 24 h of MI (ST change or LBBB) within 24 h of symptom onsetsymptom onset

TREATMENT:TREATMENT: Metoprolol 15 mg iv over 15 mins, then Metoprolol 15 mg iv over 15 mins, then 200 mg oral daily vs matching placebo200 mg oral daily vs matching placebo

EXCLUSION:EXCLUSION: Shock, systolic BP <100 mmHg, heart Shock, systolic BP <100 mmHg, heart rate <50/min or II/III AV blockrate <50/min or II/III AV block

11 OUTCOMES:OUTCOMES: Death & death, re-MI or VF/arrest up to Death & death, re-MI or VF/arrest up to 4 weeks in hospital (or prior discharge)4 weeks in hospital (or prior discharge)

Mean treatment and follow-up: 16 daysMean treatment and follow-up: 16 days

COMMITCOMMIT: Study design: Study design

Effects of MetoprololEffects of Metoprolol

Lancet. 2005;366:1622.

Death13%

P=0.0006

ReMI22%

P=0.0002

VF15%

P=0.002

Totality of Evidence (N = 52,411)COMMIT (N = 45,852)

30% relative increase in

*cardiogenic shock

*Risk factors for cardiogenic shock :heart failure, age > 70 , systolic blood pressure < 120, sinus tachycardia > 110 or heart rate < 60, increased time since onset of STEMI symptoms

Recommendations - Class Ia (B)

• ORAL beta-blocker therapy SHOULD BE initiated in the first 24 hours for patients who DO NOT have any of the following: 1) signs of heart failure,2) evidence of a low output state, 3) increased risk for cardiogenic shock, or4) relative contraindications to beta blockade

1AVB > 0.24 sec, 2nd- or 3rd-degree heart block reactive airway disease

** There is no study evaluating oral beta blockers alone

Beta-Blockers

*Risk factors for cardiogenic shock :heart failure, age > 70 , systolic blood pressure < 120, sinus tachycardia > 110 or heart rate < 60, increased time since onset of STEMI symptoms

Recommendations - Class IIa (B)

• It is reasonable to administer an IV BETA BLOCKER at the time of presentation to STEMI patients who are HYPERTENSIVE and who do not have any of the following: 1) signs of heart failure,2) evidence of a low output state, 3) increased risk for cardiogenic shock, or4) relative contraindications to beta blockade

1AVB > 0.24 sec, 2nd- or 3rd-degree heart block reactive airway disease

Beta-Blockers

*Risk factors for cardiogenic shock :heart failure, age > 70 , systolic blood pressure < 120, sinus tachycardia > 110 or heart rate < 60, increased time since onset of STEMI symptoms

Recommendations - Class III (A)

• IV beta blockers SHOULD NOT be administered to STEMI patients who have any of the following: 1) signs of heart failure2) evidence of a low output state3) increased risk* for cardiogenic shock4) relative contraindications to beta blockade

1AVB > 0.24 sec, 2nd- or 3rd-degree heart block reactive airway disease

Beta-Blockers

*Risk factors for cardiogenic shock :heart failure, age > 70 , systolic blood pressure < 120, sinus tachycardia > 110 or heart rate < 60, increased time since onset of STEMI symptoms

ReperfusionReperfusion

““Time is Muscle”Time is Muscle”

Reperfusion

• STEMI patients presenting to a hospital with PCI capability should be treated with primary PCI within 90 min of first medical contact as a systems goal. Class Ia

• STEMI patients presenting to a hospital without PCI capability, and who cannot be transferred to a PCI center and undergo PCI within 90 min of first medical contact, should be treated with fibrinolytic therapy within 30 min of hospital presentation as a systems goal, unless fibrinolytic therapy is contraindicated. Class Ib

PCI vs Fibrinolysis for STEMI:Short-Term Clinical Outcomes

75

2

6

1

7 897 7

21

2 1

5

13

5

10

15

20

25

30

35PCI

Fre

qu

ency

(%

)

P=.0002

P=.0003 P<.0001

P<.0001

P<.0001P=.0004

P=.032

P<.0001

Death Death, no shock

data

ReMI Rec.Ischemia

Total Stroke

Hem.Stroke

Major Bleed

DeathMI

CVA

Fibrinolysis

N=7739

Keeley E, et al. Lancet . 2003;361:13-20.

Brief Review of Thrombolytic Brief Review of Thrombolytic TrialsTrials

GISSI-1: Streptokinase 18% reduction in mortality at 21 d

GUSTO-1: tPA. 15% reduction in 30-day mortality compared to Streptokinase

GUSTO-3: Reteplase had no benefit over tPA but is easier to use (double bolus)

ASSENT: TNKase is similar to tPA but with less non-cerebral bleeding and better mortality with symptoms>4 hrs: Single bolus, fibrin selective, resistance to PAI-1

*Overall risk of ICH is 0.7%; Strokes occurred in 1.4%

AnticoagulantsAnticoagulants

•Patients undergoing reperfusion with fibrinolytics should receive anticoagulant therapy for a minimum of 48 hours (unfractionated heparin) or up to 8 days

•Anticoagulant regimens with established efficacy include:♥ UFH (LOE: C)♥ Enoxaparin (LOE:A)♥ Fondaparinux (LOE:B)

AnticoagulAnticoagulantant

Efficacy (through 30 d)Efficacy (through 30 d) SafetySafety Use During PCIUse During PCI

ReviparinReviparin Fibrinolysis: probably superiorFibrinolysis: probably superior

to placebo.*to placebo.*

No reperfusion: probably superior to No reperfusion: probably superior to placebo.*placebo.*

↑ ↑ risk of serious risk of serious bleeds†bleeds†

No data on reviparin alone No data on reviparin alone during PCI. Additional during PCI. Additional anticoagulant with anti-IIa anticoagulant with anti-IIa activity, such as UFH or activity, such as UFH or bivalirudin, recommended.bivalirudin, recommended.

FondaparinuxFondaparinux Fibrinolysis: appears superior to Fibrinolysis: appears superior to control rx (placebo/UFH). Relative control rx (placebo/UFH). Relative benefit vs placebo and UFH benefit vs placebo and UFH separately cannot be reliably separately cannot be reliably determined from available data.*determined from available data.*

Primary PCI: when used alone, no Primary PCI: when used alone, no advantage over UFH and trend advantage over UFH and trend toward worse outcome.toward worse outcome.

No reperfusion: appears superior to No reperfusion: appears superior to control therapy (placebo/UFH). control therapy (placebo/UFH). Relative benefit versus placebo and Relative benefit versus placebo and UFH separately cannot be reliably UFH separately cannot be reliably determined from available data.*determined from available data.*

Trend toward Trend toward ↓↓ risk of serious risk of serious bleeds†bleeds†

↑ ↑ risk of catheter thrombosis risk of catheter thrombosis when fondaparinux used when fondaparinux used alone. Additional alone. Additional anticoagulant with anti-IIa anticoagulant with anti-IIa activity, such as UFH or activity, such as UFH or bivalirudin, recommended.bivalirudin, recommended.

EnoxaparinEnoxaparin Fibrinolysis: appears superior to UFHFibrinolysis: appears superior to UFH ↑ ↑ risk of serious risk of serious bleeds†bleeds†

Enoxaparin can be used to Enoxaparin can be used to support PCI after fibrinolysis. support PCI after fibrinolysis. No additional anticoagulant No additional anticoagulant needed.needed.

Summary of Observations from Trials of Anticoagulants for STEMI

Antman EM, et al. J Am Coll Cardiol 2008. Published ahead of print on December 10, 2007. Available at http://content.onlinejacc.org/cgi/content/full/j.jacc.2007.10.001. Table 10.

Facilitated PCIFacilitated PCI

Meta-analysis: Facilitated PCI vs Meta-analysis: Facilitated PCI vs Primary PCIPrimary PCI

1.031.03(0.15-7.13)(0.15-7.13)

3.073.07(0.18-52.0)(0.18-52.0)

1.431.43(1.01-2.02)(1.01-2.02)

1.031.03

(0.49-2.17)(0.49-2.17)

Mortality Reinfarction Major Bleeding

Fac. PCIBetter

PPCIBetter

Fac. PCIBetter

PPCIBetter

Fac. PCIBetter

PPCIBetter

Keeley E, et al. Lancet 2006;367:579.

0.1 1 10 0.1 1 10 0.1 1 10

1.38 (1.01-1.87)

1.71 (1.16 - 2.51)

1.51 (1.10 - 2.08 )

Lytic alone Lytic alone N=2953N=2953

IIb/IIIa IIb/IIIa alone alone N=1148N=1148

Lytic Lytic +IIb/IIIa+IIb/IIIaN=399N=399

All All (N=4500)(N=4500)

1.40 (0.49-3.98)

1.81

(1.19-2.77)

Rescue PCI

•If evidence of cardiogenic shock, severe heart failure hemodynamically compromising ventricular arrhythmias.

•If fibriolysis has failed Evaluate 90 minutes for a <50% ST resolution in lead with greatest elevation

Summary of Acute STEMI Summary of Acute STEMI TreatmentTreatment

• Stabilize, MONA/BBStabilize, MONA/BB

• ASA if MI is even considered. ASA if MI is even considered.

• The artery is CLOSED; time is muscleThe artery is CLOSED; time is muscle

• PCI is preferred method of reperfusion PCI is preferred method of reperfusion

• Cath lab (regardless of method of reperfusion) Cath lab (regardless of method of reperfusion) ifif– Hemodynamic or electrical instabilityHemodynamic or electrical instability– Failed FibrinolysisFailed Fibrinolysis

Case PresentationCase Presentation

• 51 y.o. man with increasing shortness 51 y.o. man with increasing shortness of breath and chest pain x 60minof breath and chest pain x 60min

• Came to ED because she can no Came to ED because she can no longer walk up a flight of stairs or lay longer walk up a flight of stairs or lay down flat.down flat.

• No N/V/Diaphoresis. No LH or No N/V/Diaphoresis. No LH or dizzinessdizziness

• No known history of cardiac or No known history of cardiac or pulmonary disease.pulmonary disease.

Physical ExamPhysical Exam• Vital Signs: HR 120; BP 90/60; RR 28.Vital Signs: HR 120; BP 90/60; RR 28.

• General: Alert and oriented x 3. Mild General: Alert and oriented x 3. Mild respiratory distress.respiratory distress.

• HEENT: NC, no trauma.HEENT: NC, no trauma.

• Neck: Supple, no lymphadenopathy.Neck: Supple, no lymphadenopathy.

• Heart: Regular S1 and S2. 2/6 early SEM Heart: Regular S1 and S2. 2/6 early SEM along L sternal border (no significant along L sternal border (no significant radiation). No carotid bruits. ? JVD.radiation). No carotid bruits. ? JVD.

• Lungs: Tachypnic. Rales 1/3 up the back Lungs: Tachypnic. Rales 1/3 up the back bilaterally. Otherwise clear.bilaterally. Otherwise clear.

• Abdomen: Obese. BenignAbdomen: Obese. Benign

• Extremities: Warm. No C/C. Trace edema.Extremities: Warm. No C/C. Trace edema.

EKGEKG

Chest X-RayChest X-Ray

TreatmentTreatment

• MONA - Morphine, Oxygen, AspirinMONA - Morphine, Oxygen, Aspirin

• No nitrates because hypotensiveNo nitrates because hypotensive

• No beta-blocker b/c in heart failureNo beta-blocker b/c in heart failure

• Primary PCI – LAD occlusionPrimary PCI – LAD occlusion

Complications of Myocardial Complications of Myocardial InfarctionInfarction

• ArrhythmiasArrhythmias• Ventricular Septal PerforationVentricular Septal Perforation• Ischemic Mitral Regurgitation, Ischemic Mitral Regurgitation,

Papillary Muscle RupturePapillary Muscle Rupture• Ventricular Free Wall RuptureVentricular Free Wall Rupture• Systemic Embolism Systemic Embolism • Ventricular AneurysmVentricular Aneurysm• PericarditisPericarditis• Cardiogenic Shock (another lecture)Cardiogenic Shock (another lecture)

Ventricular ArrhythmiasVentricular Arrhythmias

•60-110 BPM; Up to 20% STEMI patients have this

•Usually a result of reperfusion; no specific therapy needed if HD stable. Otherwise, atropine or even atrial pacing may increase sinus rate to overdrive pace the AIVR

•Routine post-MI management with B-blockers, ACE, etc.

PVC’sPVC’s

• Extremely common, along with Extremely common, along with short runs of NSVTshort runs of NSVT

• Amiodarone won’t increase Amiodarone won’t increase mortality, other antiarrhythmics mortality, other antiarrhythmics (other than B-blockers) do. (other than B-blockers) do.

• B-blockers, electrolytesB-blockers, electrolytes

• Best if no antiarrhythmics are Best if no antiarrhythmics are usedused

Not So Benign RhythmNot So Benign Rhythm

•Ischemic VT is often polymorphic; HR>100-110 BPM

•Higher risk with more LV damage and in first 2 days after MI

•Treat: DCCV, cath lab (if needed), electrolyte correction, amiodarone, lidocaine, B-Blockers

If That Didn’t Make You If That Didn’t Make You Nervous…Nervous…

Primary VF: Sudden event with no warning--10% STEMI patients before lytics. MUCH MUCH less now

Secondary VF: Occurring in setting HF or shock

Late VF: >48 hrs after MI-->Increased risk with IVCD, anterior wall MI, persistent SVT early in course, and RV infarction requiring pacing

***Have to worry about structural complication (free wall rupture)/ischemia

Treat: Non-synced DCCV, electrolyte correction

Why get worked up about Why get worked up about electrolytes?electrolytes?

Nordrehaug JE, van der Lippe G: Hypokalemia and ventricular fibrillation in acute myocardial infarction. Br Heart J 50:525, 1983.

NOTE: Pre-lytic study

Sinus Bradycardia/Junctional Escape Sinus Bradycardia/Junctional Escape RhythmRhythm

• 4-5% of STEMI patients have a 4-5% of STEMI patients have a bradyarrhythmiabradyarrhythmia

• Sinus node ischemia--Blood supply to SA Sinus node ischemia--Blood supply to SA node is: 65% RCA, 25% LCX, 10% dual node is: 65% RCA, 25% LCX, 10% dual supply. supply.

• Most commonly seen in Inferior/posterior Most commonly seen in Inferior/posterior MI’s. MI’s.

• Often induced by vagal reaction that may Often induced by vagal reaction that may be protectivebe protective

Atrioventricular BlockAtrioventricular Block

• First-DegreeFirst-Degree: Usually the RCA and does not require : Usually the RCA and does not require treatment. Hold the B-blocker for PR>240 mstreatment. Hold the B-blocker for PR>240 ms

• Second-DegreeSecond-Degree: Usually RCA disease and does not require : Usually RCA disease and does not require treatment unless HR less than 50 and arrhythmia or treatment unless HR less than 50 and arrhythmia or symptoms. Otherwise, atropine or pacesymptoms. Otherwise, atropine or pace

• Third-DegreeThird-Degree: Can be from any location of infarct. Can be : Can be from any location of infarct. Can be preceded by Mobitz II Blockpreceded by Mobitz II Block– Pace for symptoms and for hemodynamic support. Usually Pace for symptoms and for hemodynamic support. Usually

not needed in inferior MI’s as block is transient (pace for not needed in inferior MI’s as block is transient (pace for HR<40-50)HR<40-50)

Post-MI VSDPost-MI VSD

• ~2% of acute MI’s prior to reperfusion era~2% of acute MI’s prior to reperfusion era

• ~0.2% in GUSTO-I streptokinase trial~0.2% in GUSTO-I streptokinase trial

• Without reperfusion, usually occurs within first Without reperfusion, usually occurs within first weekweek– Day 1--Large intramural hematomas that dissectDay 1--Large intramural hematomas that dissect– Day 3-5--Coagulation necrosisDay 3-5--Coagulation necrosis

• 24 hr or less if receive lysis--Lytics reduce infarct 24 hr or less if receive lysis--Lytics reduce infarct size but may promote hemorrhagic dissection of size but may promote hemorrhagic dissection of myocardiummyocardium

Symptoms, Exam, and DiagnosisSymptoms, Exam, and Diagnosis

• Chest pain, dyspneaChest pain, dyspnea

• PE: Harsh, holosystolic PE: Harsh, holosystolic murmur along sternal border murmur along sternal border radiating to base/apex/R radiating to base/apex/R parasternum; thrill in 1/2 parasternum; thrill in 1/2 patients; S3; Loud P2; TR.patients; S3; Loud P2; TR.

• Compared to acute MR, Compared to acute MR, murmur is loud. Up to 20% of murmur is loud. Up to 20% of patients may have MR as well patients may have MR as well thoughthough

CCU ManagementCCU Management

• IABPIABP• VentilationVentilation• Diuresis/HF ManagementDiuresis/HF Management• Inotropes (can increase shunt)Inotropes (can increase shunt)• Nitroprusside if tolerated (can cause Nitroprusside if tolerated (can cause

hypotension)hypotension)• Mortality with conservative management is Mortality with conservative management is

HIGH (24%, 46%, HIGH (24%, 46%, 67-82%67-82% at 24 hrs, 1 wk, and 2 at 24 hrs, 1 wk, and 2 months, respectively)months, respectively)

• Ultimately, mechanical closure needed (surgery Ultimately, mechanical closure needed (surgery vs. percutaneous)-TIMING is questionable but vs. percutaneous)-TIMING is questionable but clinical status should not preclude thisclinical status should not preclude this

Acute Mitral RegurgitationAcute Mitral Regurgitation

• Caused by papillary muscle ischemia or rupture Caused by papillary muscle ischemia or rupture (less likely). Rupture is usually partial since (less likely). Rupture is usually partial since total is essentially incompatible with lifetotal is essentially incompatible with life

• Usually in setting of inferior MI involving the Usually in setting of inferior MI involving the posteromedial papillary muscle (single PDA posteromedial papillary muscle (single PDA blood supply as opposed to anterolateral)blood supply as opposed to anterolateral)

• Rupture usually occurs 3-5 days post-MI and in Rupture usually occurs 3-5 days post-MI and in 1% of MI’s and requires emergent operative 1% of MI’s and requires emergent operative repair (50% mortality in 24 hrs)repair (50% mortality in 24 hrs)

• Accounts for 7% of cardiogenic shock and 5% Accounts for 7% of cardiogenic shock and 5% of mortality associated with acute MIof mortality associated with acute MI

• Area of infarction does NOT have to be largeArea of infarction does NOT have to be large

Symptoms, Exam, DiagnosisSymptoms, Exam, Diagnosis

• Symptoms: Those of Symptoms: Those of heart failureheart failure

• PE: May or may not PE: May or may not hear loud systolic hear loud systolic murmur (need a murmur (need a gradient)gradient)

CCU ManagementCCU Management

• Mechanical ventilation if neededMechanical ventilation if needed• IABP--especially for hypotensionIABP--especially for hypotension• PCI if papillary m. ischemia (not rupture)PCI if papillary m. ischemia (not rupture)• Afterload reduction (nitroprusside if Afterload reduction (nitroprusside if

possible) to MAP of 70-80 mm Hgpossible) to MAP of 70-80 mm Hg• Since mortality is 90% with medical Since mortality is 90% with medical

therapy alone, surgery is the major therapy alone, surgery is the major therapy of choicetherapy of choice– Perioperative mortality 20-25%Perioperative mortality 20-25%– Overall surgical mortality is even higherOverall surgical mortality is even higher

Free Wall Free Wall RuptureRupture

• ~10% of patients who die in ~10% of patients who die in hospital from STEMIhospital from STEMI

• Most commonly between 1 and 4 Most commonly between 1 and 4 days (up to 3 weeks)days (up to 3 weeks)

• Caused by tear or dissecting Caused by tear or dissecting hematomahematoma

• More common with fibrinolysis More common with fibrinolysis compared to PCIcompared to PCI

• More common in patients without More common in patients without previous infarctionprevious infarction

Symptoms, Exam, DiagnosisSymptoms, Exam, Diagnosis

• Acute symptoms include sudden chest pain Acute symptoms include sudden chest pain (esp with cough, strain) and sudden death(esp with cough, strain) and sudden death

• Subacute symptoms: Pericarditis-like Subacute symptoms: Pericarditis-like symptoms (chest pain, nausea, vomiting)symptoms (chest pain, nausea, vomiting)

• Exam (think HF and tamponade): JVD, Exam (think HF and tamponade): JVD, pulsus, diminished heart sounds, rub, pulsus, diminished heart sounds, rub, possibly a new murmurpossibly a new murmur

TreatmentTreatment

• Pericardiocentesis if timePericardiocentesis if time

• Surgical repair is the only treatmentSurgical repair is the only treatment

• Mortality is reasonable if Mortality is reasonable if

patient gets to the OR patient gets to the OR

in timein time

• 90% mortality without90% mortality without

surgerysurgery

Summary of Acute STEMI Summary of Acute STEMI ComplicationsComplications

• Much more rare in the reperfusion eraMuch more rare in the reperfusion era– Look for them especially in delayed presentationLook for them especially in delayed presentation

• Arrhythmias are most common complication Arrhythmias are most common complication and may require emergent treatmentand may require emergent treatment

• VSD’s, papillary muscle rupture, and free VSD’s, papillary muscle rupture, and free wall ruptures carry a VERY high mortality wall ruptures carry a VERY high mortality and require emergent surgical consultationand require emergent surgical consultation– Support mechanically until patient receives Support mechanically until patient receives

operationoperation

Other ReferencesOther References

1.1. Crawford PA, ed. The Washington Crawford PA, ed. The Washington Manual Subspecialty Consult Series: Manual Subspecialty Consult Series: Cardiology Subspecialty Consult. Cardiology Subspecialty Consult. Philadelphia: Lippincott Williams and Philadelphia: Lippincott Williams and Wilkins, 2004.Wilkins, 2004.

2.2. Griffin BP, Topol EJ, eds. Manual of Griffin BP, Topol EJ, eds. Manual of Cardiovascular Medicine, 2nd ed. Cardiovascular Medicine, 2nd ed. Philadelphia: Lippincott Williams and Philadelphia: Lippincott Williams and Wilkins, 2004Wilkins, 2004

3.3. Zipes, Libby, Bonow, Braunwald, eds. Zipes, Libby, Bonow, Braunwald, eds. Braunwald’s Heart Disease: A Textbook Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine, 7th ed. of Cardiovascular Medicine, 7th ed. Philadelphia: Elsevier Saunders, 2005 Philadelphia: Elsevier Saunders, 2005

Questions?Questions?